K2P channels regulate electrical activity in various tissues through generation of a plasma membrane background ‘leak’ potassium conductance {Enyedi, 2010; Lesage, 2011}. Channels from this family are found in both excitable and non-excitable cells and have been implicated vasodilation, respiratory control, nociception, neuroprotection, anesthesia, and anti-depressant responses {Es-Salah-Lamoureux, 2010; Enyedi, 2010; Lesage, 2011}. Due to their involvement in pain, ischemia, and migraine, K2Ps have been proposed as therapeutic targets for a range of cardiovascular and neurological disorders {Mathie, 2007 #867; Bayliss, 2008; Es-Salah-Lamoureux, 2010}; however, despite this considerable interest, the K2P family is poorly responsive to classic potassium channel blockers {Lotshaw, 2007} and remains practically pharmacologically orphaned {Es-Salah-Lamoureux, 2010; Lesage, 2011; Bayliss, 2008}. Further, the development of specific K2P pharmacology has been hindered by the scarcity of facile methods to detect potassium flux in cells and by the fact that the channels produce a ‘leak’ current that is a challenge for conventional electrophysiological screening assays. Thus, there has been a need to develop new, robust screening strategies that could identify K2P modulators. Disclosed herein, inter alia, are solutions to these and other problems in the art.